Assuntos
Purging da Medula Óssea , Receptores Frizzled , Transplante de Células-Tronco de Sangue Periférico , Neoplasias Peritoneais/terapia , Receptores Acoplados a Proteínas G , Neoplasias de Tecidos Moles/terapia , Adulto , Terapia Combinada , Humanos , Neoplasias Peritoneais/patologia , Neoplasias de Tecidos Moles/patologia , Transplante AutólogoRESUMO
BACKGROUND: Recombinant human granulocyte colony-stimulating factor (rhG-CSF) is a growth factor commonly used to avoid leukopenia after chemotherapy. Endogenous G-CSF is produced by macrophages and granulocytes that infiltrate tumors. It has been reported that rhG-CSF stimulates the proliferation of several cell lines as well as bladder carcinoma cells. Conversely, in some hematopoietic cell lines such as U-937, WEHI-3B, and K-562 no effect or in some cases a differentiation pattern was found. Moreover, the role of rhG-CSF on the proliferation of solid tumors is not well understood. METHODS: In this study, 10 ovarian carcinoma biopsies were characterized for the presence of G-CSF and G-CSF receptor by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical analysis. Proliferation was analyzed by ATP viability assays. RESULTS: Performing RT-PCR, these biopsies and four ovarian carcinoma cell lines were analyzed for endogenous G-CSF production, which was found in some biopsies and in all cell lines. Despite the presence of the G-CSF receptor in all biopsies and cell lines, no proliferation was found after rhG-CSF incubation of the cell lines or the tumor samples for 3 and for 6 days, respectively. CONCLUSIONS: Summarizing the authors' in vitro studies, rhG-CSF does not affect the proliferation of ovarian carcinoma cells in vitro.
Assuntos
Carcinoma/genética , Carcinoma/patologia , Expressão Gênica , Fator Estimulador de Colônias de Granulócitos/fisiologia , Neoplasias Ovarianas/genética , Neoplasias Ovarianas/patologia , Receptores de Fator Estimulador de Colônias de Granulócitos/genética , Trifosfato de Adenosina/análise , Biópsia , Southern Blotting , Carcinoma/química , Divisão Celular , Fatores Estimuladores de Colônias/farmacologia , Feminino , Fator Estimulador de Colônias de Granulócitos/análise , Humanos , Imuno-Histoquímica , Neoplasias Ovarianas/química , Receptores de Fator Estimulador de Colônias de Granulócitos/análise , Proteínas Recombinantes , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Células Tumorais CultivadasRESUMO
The present investigation was performed to study the effects of steroids on interleukin-6 (IL-6) production and on proliferation of human umbilical vein endothelial cells (HUVEC). HUVEC were isolated and cultured in 24-well dishes until confluency was achieved. Afterwards cells were stimulated with either 17beta-estradiol or progesterone at concentrations of 10(-12)-10(-6) mol/l. IL-6 concentrations in cell supernatants were measured by ELISA and cell proliferation was determined by flow-cytometric assessment of S-phase-cells. 17Beta-estradiol significantly inhibited basal IL-6 secretion at doses of 10(-12)-10(-6) mol/l whereas progesterone had no measurable effects. Neither 17beta-estradiol nor progesterone affected the proliferation rate of endothelial cells. The results of our study suggest that 17beta-estradiol at non-proliferative doses regulates IL-6 secretion of endothelial cells and thereby modulates processes of vascular physiology.
